The respiratory tract is constantly exposed to airborne microbes that contribute to infectious diseases, from which more than 400 million people currently suffer from. The first line of defense against these pathogens is provided by the mucosal surfaces through mucocilliary clearance and their complex and various secretions. The antimicrobial activities of proteins in these secretions have been well studied, but the contribution of the lipids to mucosal defense have not yet been fully established. Of the lipid content, cholesteryl esters (CE) have shown promising implications of antimicrobial activity. I studied different mechanistic approaches that would allow for a comprehensive study of CE`s contribution to the innate immune defense of the respiratory epithelia. I found that CI-1011 is not a viable and specific inhibitor of the gene target SOAT-1 and despite many negative results my findings will guide the next steps for studying the contribution of cholesteryl esters to the immune defense of the host in in vitro models. Furthermore, my study provides new evidence that lipid metabolism and the innate immune response are linked by shared signaling pathways. This research could possibly provide an alternative therapeutic and prophylactic approach to treating respiratory infectious diseases, and possibly delay the development of new antibiotic-resistant strains.